1. Academic Validation
  2. The phosphorylation status of Hsp82 regulates mitochondrial homeostasis during glucose sensing in Saccharomyces cerevisiae

The phosphorylation status of Hsp82 regulates mitochondrial homeostasis during glucose sensing in Saccharomyces cerevisiae

  • J Mol Biol. 2023 Apr 15;168106. doi: 10.1016/j.jmb.2023.168106.
Guanzu Peng 1 Kaiyu Hu 1 Xuan Shang 1 Wanjie Li 2 Fei Dou 3
Affiliations

Affiliations

  • 1 Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China.
  • 2 Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China. Electronic address: lwj@bnu.edu.cn.
  • 3 Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, China. Electronic address: douf@bnu.edu.cn.
Abstract

Sensing extracellular glucose, budding yeast switches from aerobic glycolysis to Oxidative Phosphorylation to adapt to environmental changes. During the conversion of metabolic mode, mitochondrial function and morphology change significantly. Mitochondria are the main supply factories of energy for various life activities in cells. However, the research on the signal pathways from glucose sensing to changes in mitochondrial function and morphology is still scarce and worthy of further exploration. In this study, we found that in addition to the known involvement of molecular chaperone Hsp82 in stress response during the conversion of metabolic mode, the phosphorylation status of Hsp82 at S485 residue regulates mitochondrial function and morphology to maintain mitochondrial homeostasis. The Hsp82S485A mutant that mimics dephosphorylation at S485 residue showed abnormal growth phenotypes related to mitochondrial defects, such as the petite phenotype, slow growth rates, and inability to use non-fermentable carbon sources. Further exploring the causes of growth defects, we found that the Hsp82S485A mutant caused mitochondrial dysfunction, including a decrease in cellular oxygen consumption rate, defects in mitochondrial electron transport chain, decreased mitochondrial membrane potential and complete loss of mtDNA. Furthermore, the Hsp82S485A mutant displayed fragmented or globular mitochondria, which may be responsible for its mitochondrial dysfunction. Our findings suggested that the phosphorylation status of Hsp82 at S485 residue might regulate mitochondrial function and morphology by affecting the stability of mitochondrial fission and fusion-related proteins. Thus, Hsp82 might be a key molecule in the signal pathway from glucose sensing to changes in mitochondrial function and morphology.

Keywords

Hsp82; glucose sensing; mitochondrial function; mitochondrial morphology; phosphorylation.

Figures
Products
Inhibitors & Agonists
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-15534
    99.0%, Mitochondrial Membrane Potential Probe
Other Products